The Bax subfamily of Bcl2-related proteins is essential for apoptotic signal transduction by c-Jun NH2-terminal kinase

被引：430

作者：

Lei, K

Nimnual, A

Zong, WX

Kennedy, NJ

Flavell, RA

Thompson, CB

Bar-Sagi, D

Davis, RJ

机构：

[1] Univ Massachusetts, Sch Med, Program Mol Med, Howard Hughes Med Inst, Worcester, MA 01605 USA

[2] SUNY Stony Brook, Dept Mol Genet & Microbiol, Stony Brook, NY 11794 USA

[3] Univ Penn, Sch Med, Abramson Family Canc Res Inst, Dept Canc Biol, Philadelphia, PA 19104 USA

[4] Yale Univ, Sch Med, Howard Hughes Med Inst, New Haven, CT 06520 USA

[5] Yale Univ, Sch Med, Immunobiol Sect, New Haven, CT 06520 USA

来源：

MOLECULAR AND CELLULAR BIOLOGY | 2002年 / 22卷 / 13期

关键词：

D O I：

10.1128/MCB.22.13.4929-4942.2002

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

摘要：

Targeted gene disruption studies have established that the c-Jun NH2-terminal kinase (JNK) signaling pathway is required for stress-induced release of mitochondrial cytochrome c and apoptosis. Here we demonstrate that activated JNK is sufficient to induce rapid cytochrome c release and apoptosis. However, activated JNK fails to cause death in cells deficient of members of the Bax subfamily of proapoptotic Bcl2-related proteins. Furthermore, exposure to stress fails to activate Bax, cause cytochrome c release, and induce death in JNK-deficient cells. These data demonstrate that proapoptotic members of the Bax protein subfamily are essential for JNK-dependent apoptosis.

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收藏

页码：4929 / 4942

页数：14

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